We are continuing our effort to evaluate the physiological role of our purified serum-immunosuppressive factor, which we have termed "suppressive E-receptor (SER)" factor. SER acts to inhibit the proliferation of growth-factor-dependent normal B or T cells in culture, i.e., BCGF-dependent human B-cell line BD-7 and TCGF-dependent murine T-cell line, CT-6. With the same manner, it also inhibited the production of IL-1 and IL-2 from normal human macrophages and T lymphocytes upon stimulation with lipopolysaccharide and phytohemagglutinin, respectively. However, SER did not interfere with the activities of IL-1 or IL-2 once they were produced. This inhibitory effect of SER on cell proliferation can be demonstrated by its direct inhibition on DNA-polymerase of phytohemagglutinin-stimulated, normal human T lymphocytes. Consequently, the inhibitory effect of SER on IL-1 and IL-2 production cannot be reversed by exogenous addition of IL-1 or IL-2. In our attempt to elucidate the immunochemical or biochemical relationship between the SER factor and the E-receptor of human T lymphocytes, we are cloning the E-receptor from human T-lymphoma cell line. During the course of developing a radioimmunoassay on SER using anti-E-receptor antibody, we learned that T11 antibody fortuitously binds to SER factor. Therefore we are in the process of developing a monoclonal antibody specifically directed to SER factor. (HF)